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Anorexia is defined as the absence of appetite despite the proximity of available food sources, and the presence of negative energy balance. It is manifest as a significant decrease in food intake, which usually results in a loss of body weight. In humans, anorexia can both accompany and represent the primary symptom of various psychological or physiological pathologies. To understand anorexia, regardless of its cause, locus of origin, or intensity, we must understand the neural and physiological mechanisms that regulate the initiation and termination of feeding behavior. To approach this issue, we employ a rodent model of anorexia, which develops as an adaptive response to the homeostatic challenge of dehydration (DE). To generate DE, rats are deprived of drinking water and only allowed access to hypertonic saline to drink for a course of five days, and, although chow is freely available during this time, rats voluntarily limit their food intake, and anorexia ensues.; Using this rodent model of anorexia, we present a series of experiments that examine what specific components of food intake are altered following DE. First, following detailed meal pattern analysis, we determined that DE-anorexia in rats results as a function of decreased meal size, while the number of meals initiated daily remains predominantly unaltered. We then investigated how DE affects the feeding that follows manipulation of the nucleus accumbens shell (ACBsh), a ventral pallidal region shown to regulate various aspects of food intake, including feeding initiation and ingestion of palatable food. Consistent with the results from the meal pattern analysis, we found that although DE significantly attenuates overall food intake, the ability of ACBsh manipulation to initiate feeding remained unaltered between normal and DE states. We also observed that DE does not alter the ability rats to differentiate between palatable and normal chow, nor does it alter the preference for palatable chow. Finally, in this thesis we closely investigated the ingestive behavioral patterns that occur following the reversal of DE rats. The results of these experiments support the hypothesis that DE targets the ingestive behavior control column of the hypothalamus to produce anorexia, and that the descending projections of the hypothalamus to the hindbrain might contribute to the heightened satiation observed in DE rats.